Severe Dehydration Trigger of Disseminated Intravascular Coagulation in a 93-Year-Old Man with an Abdominal Aortic Aneurysm.

Abstract

A 93-year-old man was brought to the hospital because of failure to thrive and poor oral intake. He had dementia and, for 5 days before admission, had refused to eat and drink. He had a past medical history of diverticulosis, hypertension, and an abdominal aortic aneurysm (AAA). Blood pressure on admission was 130/80 mm Hg, pulse rate was 90 beats per minute, oxygen saturation was 98% on room air, and body temperature was normal. On physical examination, he was severely dehydrated, with dry mucosa and orthostatic hypotension. A large pulsating mass was palpable in the abdomen. Laboratory results indicated mild anemia (hemoglobin 12.1 g/dL), thrombocytopenia (platelet count 108,000/uL), hypernatremia (sodium 155 mmol/L), acute kidney injury (creatinine 3.5 mg/dL), high serum osmolality (346 mosm/kg), and normal liver function (albumin 2.9 g/dL). He was admitted with a diagnosis of severe dehydration, hypernatremia, and acute kidney injury. Renal ultrasound did not show any hydronephrosis or obstruction. Abdominal computed tomography CT revealed infrarenal AAA (maximum diameter 6 cm) with a mural thrombus that extended into the common iliac arteries. No significant change in the size of the aneurysm was reported from CT from the previous year. The only new finding was an intraluminal thrombosis. He was uncooperative, refused oral feeding, and removed his intravenous line multiple times. On the second day after admission, laboratory results revealed a significant drop in platelet count (65,000/uL) without improvement in hypernatremia and worsening kidney function. Coagulation studies found abnormal coagulation factors (prolonged prothrombin time (PT) and partial thromboplastin time (PTT), hypofibrinogenemia (50 mg/dL), high fibrinogen degradation products (>40 mg/dL), high D-dimer (17.14 mg/L), low factor VIII activity (75%), high lactate dehydrogenase (469 U/L), low haptoglobin (<10 mg/dL). Schistocytes were seen in the peripheral blood smear. He was transferred to medical intensive care unit with a diagnosis of disseminated intravascular coagulation (DIC). Blood culture was negative. No infiltration was reported on chest X-ray. During admission, he remained afebrile with stable blood pressure and no leukocytosis. He received 3 U of cryoprecipitate. Four days later, after hydration and improvement of hypernatremia, coagulopathy improved significantly. Eleven days after admission, he had normal PT and fibrinogen level, platelets had increased to 133,000/uL, and creatinine had decreased to 1.7 mg/dL. Laboratory data led to a diagnosis of DIC, with AAA as the only identifiable cause of the coagulopathy. His family refused surgical repair of the AAA and oral anticoagulation, and he was discharged home on aspirin. Follow-up laboratory results after 1 month showed normal PTT, PT, and fibrinogen level and an increase in platelets to 150,000/uL. Worldwide, people have been living longer, which has resulted in an increase in the demands on the healthcare system for the aging population with atherosclerotic diseases, which includes aortic aneurysms. Chronic DIC is a well-known complication of aortic aneurysm. Consumptive coagulopathy and thrombus within the aneurysm is not an infrequent finding. Waxing and waning coagulopathy has been reported for years in individuals who did not undergo surgical repair of an aneurysm.1 A high index of clinical suspicion of a coagulation disorder should be maintained in elderly adults with AAA. DIC secondary to an aortic aneurysm was reported in 1967.2 In preoperative evaluation of individuals with aortic aneurysms, 40% have high levels of D-dimer, and 4% have clinically overt DIC.1-3 The pathophysiology of DIC in association with AAA remains unclear. It has been postulated that exposure of subendothelial tissues of the aneurysm leads to deposition of platelets and fibrin. As the aneurysm gradually expands, a compensated state of secondary fibrinolysis and low-grade DIC is seen in approximately 40% of individuals. Additional factors such as hepatic disease, renal insufficiency, or the rapid expansion of the aneurysm can further change the balance between coagulation and fibrinolysis and lead to clinical DIC. Continuous deposition of platelets and fibrin within the aneurysmal sac and concurrent fibrinolysis may be responsible for the consumption coagulopathy associated with some AAA. Chronic intraluminal thrombosis with activation of the inflammatory pathway has an important role in the pathogenesis of DIC.4-7 Investigations for sepsis, occult neoplasia, and liver disease were negative for the individual described herein. In spite of a nonsignificant change in aneurysm dimension, a new mural clot was reported. The only identifiable cause of coagulopathy in this man was AAA. It is likely that severe dehydration and hemoconcentration triggered intraluminal thrombosis and activation of the coagulopathy cascade. The man responded well to hydration, and his coagulopathy resolved. Conflict of Interest: The authors declare no competing interests. Author Contributions: All authors: manuscript preparation. Sponsor's Role: N/A.